Imaging of Renovascular Disease

Imaging of Renovascular Disease Ravinder Sidhu, MD,* and Mark E. Lockhart, MD, MPH† A variety of different imaging techniques have been used for the diagnosis of renal vascular diseases. The wide range of renal vascular diseases include congenital renal artery and vein variations, aneurysms, arteriovenous malformations (AVMs), renal artery stenosis, renal vein thrombosis, vasculitis, and traumatic injuries, such as dissection and vascular pedicle injury. In this article, we discuss the role of invasive and noninvasive imaging in each of these abnormalities and their typical features. Because renal artery stenosis is an important vascular abnormality encountered in clinical practice, imaging of this entity will be emphasized. Semin Ultrasound CT MRI 30:271-288 Published by Elsevier Inc.

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n recent years, the use of cross-sectional imaging for the diagnosis of disease has experienced large increases. The proliferation of computed tomography (CT) and magnetic resonance imaging (MRI) has likewise extended to the detection of genitourinary abnormalities, in addition to ultrasound. This article discusses the roles of different imaging modalities specifically for the diagnosis of renal vascular disease.

Renal Vascular Variants Multiple Renal Arteries Both kidneys are supplied by renal arteries that usually arise from the aorta. Each kidney has a single artery in most patients. Multiple renal arteries are present in 25%-40% of patients (Fig. 1) and are bilateral in approximately 10%-12%.1-4 Multiple arteries are more common on the left (31% vs. 20%).2 The left renal artery courses posterior to the left renal vein, and the right renal artery usually passes posterior to the inferior vena cava. Single renal arteries originate from the aorta at the level of L1 to L2, whereas supernumerary renal arteries may have various origins. Unusual origin sites include common iliac, superior mesenteric, inferior mesenteric, spermatic, ovarian, right colic, supraceliac aorta, and the contralateral renal arteries.5 Several terms have been used to describe multiple renal *Division of Cross-Sectional Imaging, Department of Imaging Sciences, University of Rochester School of Medicine and Dentistry, Rochester, NY. †Department of Radiology, University of Alabama at Birmingham, Birmingham, AL. Address reprint requests to Ravinder Sidhu, MD, Division of Cross-Sectional Imaging, Department of Imaging Sciences, PO Box 648, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642. E-mail: [email protected]

0887-2171/09/$-see front matter Published by Elsevier Inc. doi:10.1053/j.sult.2009.04.002

arteries, including aberrant, ectopic, accessory, polar, supernumerary, and supplementary. The term accessory artery is used to describe any renal artery other than the main renal artery. Accessory renal arteries are one of the most common clinically important vascular variants. Usually, an accessory renal artery courses into the renal hilum to perfuse the upper or lower renal pole. Three-dimensional (3D) CT angiography with volume-rendered images has shown a high sensitivity (approaching 100%) in the detection of renal arteries.6,7 However, an aberrant renal artery may arise from sources other than aorta. Similar to the origin of accessory arteries, they can be either polar or hilar.

Agenesis of the Renal Artery An absent renal artery, for all practical purposes, is associated only with renal agenesis. In such cases the adrenal gland, often still present, receives its blood supply directly from the aorta. The adrenal will generally have a discoid appearance unlike the normal triangular or Y-shape in patients who have had surgical removal of the kidney. Although a renal artery is generally present in dysgenesis as well as in renal atrophy, these vessels may be extremely atretic and may not be opacified on angiography.

Secondary Ureteropelvic Junction Obstruction Occasionally, a hilar accessory artery may significantly compress the ureteropelvic junction, leading to obstruction. A hilar artery in association with hydronephrosis can be seen in 29%-46% of patients with ureteropelvic junction obstruction (UPJ) obstruction.8,9 The crossing vessel is usually located anterior to the UPJ obstruction. However, posterolateral location of the vessel can be seen in 5%-10% of patients. CT angiography can discern the position of the crossing vessel 271

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Figure 1 Multiple renal arteries. (A) Coronal maximum intensity projection image of CTA in a renal donor depicts the fine anatomical details of multiple right renal arteries. (B) Volume-rendering reconstruction shows similar findings. (Color version of figure is available online.)

Renal Vein Variants

Left Renal Vein The left renal vein is longer than the right renal vein and averages 84 mm in length (range, 60-110 mm).13 The left renal vein is joined by the adrenal, gonadal, lumbar, and hemiazygous veins before crossing the aorta. The left renal vein occurs as one of the following types: preaortic, retroaortic, or circumaortic.

Anomalies of the renal veins may be associated with congenital anomalies of the inferior vena cava and kidneys. Accurate assessment of renal venous anatomy and its congenital variation is important before renal venous sampling, preoperative evaluation of renal donors, splenorenal shunt placement, vena cava filter placement, nephrectomy, aortic surgery, and staging of renal cell carcinoma. During the development of the inferior vena cava, there are anastomotic communications between subcardinal and supracardinal channels, which form a collar of veins around the aorta. The ventral portion of the circumaortic collar persists, thus representing the normal left renal vein. If the dorsal portion of this collar persists, the left renal vein travels posterior to aorta, forming a retroaortic left renal vein. The circumaortic left renal vein is formed by persistence of both the dorsal and the ventral portions.10,11 Overall, major left venous variants are present in 5%-11% of patients, and they are even more common in the right renal vein (20%).2,12

Preaortic Left Renal Vein Preaortic left renal vein is seen in 80%-94% cases. It courses horizontally or slightly craniad, anterior to the aorta, and enters the left side of the inferior vena cava (IVC) at the level of the L1-2 interspace. Compression of the left renal vein between the adjacent normal anatomical structures is termed “nutcracker phenomenon.” This leads to increased pressure in the left renal vein, resulting in congestion of the left kidney and venous communications, which can present as hematuria (Fig. 2).14,15 The anterior nutcracker phenomenon is the compression of the left renal vein between the aorta and the superior mesenteric artery (Fig. 3). The posterior nutcracker phenomenon results from decreased space between the aorta and the vertebra, thus causing compression if there is a retroaortic left renal vein.

and has a reported sensitivity of 100% and specificity of 96.6% for detection of arteries crossing the UPJ region.9 It is important to identify a crossing vessel leading to UPJ obstruction because vascular injury associated with endoscopic procedures can be seen up to 10% of cases.8

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Figure 2 Lumbar renal venous collateral. (A) Contrast-enhanced axial CT image in patient with hematuria shows left venous outflow through a dilated left ascending lumbar vein (arrowheads) instead of drainage into the inferior vena cava. (B) Axial FIESTA flow-sensitive MR sequence through the same level shows high signal intensity flow in the collateral vessel (arrowheads).

Retroaortic Left Renal Vein Retroaortic left renal vein results from persistence of the dorsal arch of the renal collar (Fig. 4A). The reported incidence varies from 2% to 3% of patients.1 A retroaortic left renal vein usually drains into the lower lumbar portion of the inferior vena cava. In some cases, the drainage can be into the iliac vein. On unenhanced CT, retroaortic left renal vein should be considered in the differential diagnosis of retroperitoneal lymphadenopathy, but its smooth linear appearance should

suggest the diagnosis. On contrasted CT or MRI (Fig. 5), the appearance should be unambiguous. Circumaortic Left Renal Vein A circumaortic left renal vein occurs due to persistence of the dorsal limb of the embryonic left renal vein and of the dorsal arch of the renal collar. The circumaortic left renal vein may be overlooked, with an incidence of 7%-9%.1,16 Two left renal vein components are present (Fig. 6). The superior renal vein receives the left adrenal vein and crosses anterior to the aorta. The inferior renal vein receives the left gonadal vein and crosses posterior to the aorta often approximately 1-2 cm inferior to the normal anterior vein (Fig. 4B). Again, one should be cautious not to misinterpret this structure as adenopathy.

Renal Vein Varix

Figure 3 Anterior nutcracker syndrome. Contrast-enhanced axial CT image in female with abdominal pain demonstrates narrowing of the left renal vein (black arrow) between the aorta and superior mesenteric artery. Incidental right ureteropelvic junction obstruction is noted on right side (arrowheads).

Renal varices can be idiopathic or associated with renal vein thrombosis, obstruction, or congenital anomalies of inferior vena cava or azygous vein. Idiopathic renal varix is more common on left side.17,18 Extrarenal varices (Fig. 7) are more common than intrarenal and may involve the gonadal vein. Calcification can be seen in varix and is more common in extrarenal type of varix. Varices are usually asymptomatic. However, pain and hematuria can be presenting features. A renal vein varix may mimic renal or urothelial neoplasm, hemangioma, blood clots, pyelo-ureteritis cystica, leukoplakia, granulomatous disease as tuberculosis, and radiolucent calculi. It is important to recognize this entity to avoid unnecessary nephrectomy.19,20 When a rounded soft-tissue

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Figure 4 Left renal vein variants. (A) Schematic illustration of a retroaortic left renal vein illustrates a single left renal vein coursing posterior to the aorta. LRV, left renal vein; IVC, inferior vena cava. (B) Similar depiction shows the configuration of a circumaortic renal vein. (Color version of figure is available online.)

density mass is seen on unenhanced CT either in or contiguous to the renal hilum, a renal vein varix must be excluded. Doppler ultrasound, MRI, or dynamic contrast-enhanced CT should be performed to exclude a renal varix as the cause.

Imaging Methods The diagnostic methods for renal vascular disease include invasive methods as venography and arteriography. With the advancement of recent noninvasive techniques, such as Doppler ultrasound, CTA, magnetic resonance arteriography (MRA), and magnetic resonance venography, invasive methods are less commonly needed. Color Doppler is useful as an initial method especially in a setting of good acoustic window and in expert hands. MRA and magnetic resonance venography are expensive modalities with prolonged scan time and of limited value in uncooperative patients due to sensitivity to motion artifacts. It requires specific timing of the bolus to

Figure 5 Retroaortic left renal vein. Contrast-enhanced axial T1weighted MR image demonstrates the left renal vein (LRV) with mild narrowing (arrow) as it courses behind the aorta (A).

obtain a good view of the arteriogram and venogram. With recent advances in technology, multidetector CT with 3D volume-rendering techniques is the modality of choice. Venous anomalies can be seen in axial contrast-enhanced images. However, multiplanar reconstruction techniques serve as a road map for surgical planning in oncological patients or renal donation.

Renal Artery Stenosis Renal artery stenosis occurs in fewer than 5% of adult patients with hypertension.21 However, this remains the commonest curable cause of hypertension. Therefore, it is important to identify an accurate, noninvasive screening investigation for the detection of renal artery stenosis in hypertensive patients. A variety of etiologies may be responsible for renal artery stenosis (Table 1). Atherosclerotic disease is the most common pathologic condition of renal arteries. This disease is more predominant beginning in middle age and more common among men. The atherosclerotic disease of the renal arteries is a manifestation of generalized atherosclerosis that also involves coronary, cerebral, and peripheral vessels. The disease may initially be asymmetric. In patients with coronary artery disease, the prevalence is 15% and bilateral in 3% of cases.22 The stenosis typically results from atherosclerotic plaque and calcification; it usually involves the ostium and proximal renal artery. Fibromuscular dysplasia is the second most common cause of renal artery stenosis. In renal donors, the prevalence is 2%-4%.1,23 This is predominantly seen in young or middleaged women. The lesions typically involve mid or distal main renal artery, in contrast to more proximal involvement in atherosclerosis. Bilateral involvement can be seen in twothirds of patients, more common in the setting of familial involvement. Fibromuscular dysplasia is defined according

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Figure 6 Circumaortic left renal vein. (A) Contrast-enhanced axial CT shows a superior component of the left renal vein coursing anterior (arrow) to the aorta (A). IVC, inferior vena cava. (B) At a more caudal level, a posterior component is identified behind the aorta (black arrow).

to the involvement of the vessel wall. The most common type is medial fibroplasias, which has alternating areas of narrowing and dilatation thus giving a classical “string of beads” appearance on angiography (Fig. 8).

therapeutic approaches. Over the years, various noninvasive diagnostic methods, such as duplex Doppler, power Doppler, renal scintigraphy, computed tomographic angiography (CTA), and MRA have been evolved.

Imaging Methods

Grayscale Ultrasound

Many different imaging modalities have been used for the diagnosis of renal artery stenosis. Conventional arterial catheter angiography is considered the reference standard diagnostic test for renal artery stenosis. However, it is invasive, involves ionizing radiation, and requires administration of intravascular contrast. Hence, a reliable noninvasive diagnostic test is needed to select patients for invasive diagnostic and

Conventional B mode demonstrates the anatomy of the kidney and also accurately assesses its size. It was long accepted that a reduction in renal size was associated with renal artery stenosis. Nineteen percent of patients with greater than 60% stenosis of the main renal artery will sustain a reduction in renal length of at least 1 cm during a 1-year follow-up period.24 Kidney length is measured as a surrogate for assessing

Figure 7 Renal vein varix. (A) Unenhanced axial CT in a cirrhotic male shows splenomegaly, ascites, and round soft-tissue density in retrocaval region, possibly lymph nodes (arrow). (B) On portal venous phase, presumed nodes show contrast opacification and follow the course of right renal vein (arrow), thus representing renal varix. A, aorta; IVC, inferior vena cava.

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276 Table 1 Etiologies of Renal Artery Stenosis Atherosclerosis Fibrodysplasia Medial fibroplasia (fibromuscular hyperplasia) Intimal fibroplasia Perimedial fibroplasia Adventitial fibroplasia Periarterial fibroplasia Spontaneous renal artery dissection Syphilitic aortitis Takayasu’s arteritis Thromboangitis obliterans Moyamoya disease Neurofibromatosis Congenital stenosis Entrapment of renal artery by crux of diaphragm Association with pheochromocytoma

renal parenchymal mass, which depends on the number of functioning nephrons. However, the diagnostic criteria of renal length is not very accurate due to the following: (1) wide variation in normal renal length between subjects; (2) reduction in renal length and volume in normal subjects over 70 years of age due to a decrease in the number of glomeruli and a reduction in the mass of the juxtamedullary nephrons24; (3) decrease in renal length caused by other chronic renal parenchymal diseases.

Doppler Ultrasound Doppler ultrasound has become much more widely available and is easier to use, noninvasive, non-ionizing, and nonnephrotoxic because no contrast administration is required. However, this technique requires expertise and may have technical difficulties in obese patients. Patients should be fasting to reduce bowel gas in an effort to improve direct visualization of the renal arteries. The main renal artery can

Figure 8 Fibromuscular dysplasia. Contrast-enhanced axial CT image shows irregular, beaded appearance (arrowheads) of right renal artery, suggestive of medial fibroplasia.

Table 2 Suggested Doppler Parameters of Renal Artery Stenosis26,27 Peak systolic velocity greater than 180-200 cm/s Spectral broadening Ratio of peak renal artery velocity to peak aortic velocity greater than 3.5 No detectable blood flow (high-grade vs. occlusion) An acceleration time greater than 0.07 s Slope of systolic upstroke less than 3 m/s2 Loss of early systolic peaks

be visualized by 2 scanning planes. In supine position, one can demonstrate the origin and proximal course of the main and accessory renal arteries. Use of an epigastric transverse scan plane helps to identify the main renal arteries, which arise laterally (anterolateral on right, posterolateral on left) from the abdominal aorta approximately 1 cm inferior to the origin of superior mesenteric artery. Intrarenal vessels can be seen with the patient in lateral decubitus position and blood flow should be recorded in the superior third, middle third, and inferior third of each kidney. Normal kidneys have a low-resistance vascular bed; thus, the Doppler spectral waveform from a normal kidney is that of a constant forward diastolic flow. The peak systolic velocity (PSV) in renal arteries without significant stenosis averages 146 ⫾ 49 cm/s. The ratio of renal artery peak velocity to aortic peak velocity is normally 2.1 ⫾ 0.8.25 There are 2 ways to evaluate disturbances in renal arterial flow due to renal artery stenosis: (1) direct visualization of renal artery stenosis seen as abnormal Doppler signals at or just distal to the stenosis; or (2) indirect visualization by abnormal Doppler signals in the intrarenal vasculature, which can be virtually visualized in all patients. The diagnosis is often made using a combination of parameters (Table 2). Significant renal artery stenosis produces an increased PSV at or immediately distal to the area of narrowing (Fig. 9); numerous threshold parameters have been suggested. In reviews of Doppler criteria, both Strandness and Stavros suggested a 180 cm/s threshold for diagnosis of 60% stenosis.26,27 Subsequently, Olin et al used a threshold of 200 cm/s for 60% stenosis.25 De Cobelli et al in 2000 have considered PSV of 100-200 cm/s as suggestive of mild stenosis (⬍50% narrowing) and those with higher than 200 cm/s as suggestive of severe stenosis (50%-99% narrowing).28 It is difficult to visualize the main renal artery in its entire course especially in obese patients and when there is a poor acoustic window secondary to bowel gas. It has been reported that main renal arteries may not be seen in approximately 42% of patients.29 Accessory renal arteries may be difficult to detect and can reduce the sensitivity of ultrasound for stenosis; approximately half of accessory renal arteries may go undetected by Doppler.30 For these patients, Handa et al in 1986 observed that changes occur in the waveform pattern of the intrarenal vessels distal to renal artery stenosis.31 To best visualize these changes, a flank approach is used to lessen the distance from transducer to kidney, and the angle of insonation of the segmental artery is maintained as

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Figure 9 Renal artery stenosis. (A) Longitudinal duplex Doppler of the left kidney in patient with previous right renal artery stent demonstrates turbulent flow with elevated PSV 477 cm/s. (B) Spectral Doppler waveform of the aorta has PSV 40 cm/s, yielding a renal artery-to-aorta ratio of 11.9. (C) Segmental artery waveform is consistent with a classic tardus-parvus morphology. (D) Catheter angiography confirms presence of high-grade left renal artery stenosis (arrow). Right artery stent is also visible without stenosis. (Color version of figure is available online.)

close to 0 degrees as possible to optimize the waveform signal. Normally, there is a steep upstroke in systole with a second small peak in early systole. Slow rise to small PSV with loss of normally occurring early systolic peak is known as tardusparvus phenomenon (Fig. 9C). Delayed upstroke can be measured by acceleration time (time from the start of systole to peak systole), and acceleration index (slope of the systolic upstroke). An acceleration time greater than 0.07 seconds with a tardus-parvus pattern indicates severe stenosis of the extrarenal arteries. The results of Doppler studies are variable and depend somewhat on the criteria selected. Sensitivity up to 92% and specificity up to 95% for detection of severe renal artery stenosis greater than 70% have been reported.32,33 For 50%

stenosis, a combination of PSV ⬎180 cm/s, distal main renal artery velocity less than one-fourth of peak velocity, or acceleration time ⬎0.07 seconds yielded a sensitivity of 96.7% and specificity of 98%.34 Power Doppler imaging has emerged as a complementary new tool for the detection of blood flow and can be used to compensate for a few of the limitations of conventional Doppler imaging. The major advantages of power Doppler are (1) the output is angle independent and thus relatively unaffected by directional changes in the imaged vessels and (2) power Doppler is more sensitive in the detection of slow flow and low-velocity vessels. However, the most important drawback of power Doppler is motion sensitivity. Helenon et al in 1998 reported a series of 49 patients in whom power Doppler led to a change in the final diagnosis in 13 cases

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(26.5%), including 12 cases of nonstenotic atherosclerotic plaques and 1 case of subocclusive high-grade renal artery stenosis without detectable flow on conventional color Doppler ultrasound that was misdiagnosed as an occlusion.35

Computed Tomographic Angiography CTA has emerged as a reliable, noninvasive method for imaging of the renal vasculature. With the advent of spiral CT, the diagnostic accuracy for renal artery stenosis has increased markedly to above the mid 90th percentile.7 Multidetector CT allows the acquisition of multiple contiguous slices through an area of interest during a single breath-hold that provides sufficient data to reconstruct 3D images. Various protocol techniques are available. However, the general agreement is that a timed bolus and rapid injection rate are essential for high image quality. Three techniques used for reconstruction are maximum-intensity-projection (MIP), shaded-surface display, and volume rendering. Both MIP and volume-rendering techniques are complementary in the CTA evaluation of renal artery stenosis. Axial images alone may be inadequate because renal arteries are known to have a tortuous and variable course. The volumetric data possible by CTA can allow demonstration of the renal arteries in multiple planes and projections.21 Normal results from CTA virtually rule out renal artery stenosis.6 Furthermore, CTA can give additional information about the state of vessel wall, including mural calcification and plaques. Detailed evaluation with source and volume-rendering images is crucial because the severity of atherosclerotic calcified plaques is underestimated or obscured by MIP-rendering techniques. Volume-rendering images are also more useful in cases of overlapping vessels.36 In 1 study, CTA with real-time interactive volume rendering had a specificity of 99%, whereas maximum intensity projection had a specificity of 87% for renal artery stenosis.6 CTA can also demonstrate secondary signs of renal artery stenosis, such as poststenotic dilatation, delayed nephrographic progression of enhancement in the affected kidney, and renal parenchymal changes of atrophy. The contralateral kidney can be used as a standard of reference provided the contralateral kidney is normal. CTA is also helpful in the detection of accessory renal arteries, which are difficult to evaluate on Doppler ultrasound and may commonly have false-negative results. CTA also plays important role in the evaluation of renal stent grafts; highly attenuating graft material and the intraluminal contrast material can be usually distinguished.7 However, if the renal function has been compromised, a major drawback of CTA is the potential nephrotoxicity of iodinated intravenous contrast media. Ionizing radiation exposure is also an increasing concern, especially in the young and the pregnant patients.

Magnetic Resonance Angiography MR angiography is emerging as a promising noninvasive investigation and is fast becoming a clinical standard for the detection of renal artery stenosis. Unenhanced examination includes 2 basic MR angiography techniques: time-of-flight

Figure 10 Renal artery stenosis. Contrast-enhanced MR angiography shows focal narrowing of the proximal left renal artery (arrow), using coronal maximum intensity projection view.

(TOF) MR angiography, and phase-contrast (PC) MR angiography techniques, which allow evaluation of the renal arteries and other visceral arteries. Both are flow-sensitive techniques and can be acquired in either 2D or 3D formats. In TOF MR angiography, the contrast between flowing blood and the adjacent stationary tissue depends on the inflow of fully magnetized protons into a preselected volume of saturated stationary tissue.37 PC MR angiography relies on the phase change induced in moving spins as they pass through a magnetic field gradient. PC MR angiography not only gives anatomical information but also allows direct quantitative evaluation of flow dynamics with the intensity of flow signal being related to flow velocity.38 In both of these techniques, post processing with MIP or surface rendering is required for detection of areas of stenosis, which are seen as signal voids or areas of narrowing. The administration of gadolinium chelate paramagnetic contrast agents increases the diagnostic performance of MR angiography, similar to CTA in a recent direct comparison.39 Contrast-enhanced MR angiography requires breath-holding but has a higher sensitivity for detecting stenosis in main and accessory renal arteries (Fig. 10). Contrast-enhanced MR angiography not only demonstrates anatomic information of vascular stenosis but also provides some information about the functional significance of a stenosis. Contrast-enhanced 2D MR angiography has a sensitivity of 92%-100% and a specificity of 92%-93% for the detection of main renal artery stenosis greater than 50%40 but is suboptimal for the detection of hemodynamically significant lesions of distal, intrarenal, and accessory renal arteries. 3D TOF sequences have been reported to have higher detection rate for accessory renal arteries.41 Contrast-enhanced 3D MR angiography has a

Renovascular imaging slightly higher sensitivity and specificity in diagnosing stenosis greater than 50%.42,43 Gadolinium contrast agents have been recently linked to the development of nephrogenic systemic fibrosis but the risk of various agents and clinical settings is still being considered. Various institutions have created glomerular infiltration rate guidelines for administration of gadolinium, but there is no current consensus. Other contraindications to MR include pacemakers, certain ferromagnetic aneurysms or hemostatic clips, valve replacements, and metallic intraorbital foreign bodies.

Nuclear Imaging In 1983, Majd et al described the effect of angiotensin-converting enzyme (ACE) inhibitor on renal artery stenosis. They observed no radionuclide uptake on diethylene triamine pentaacetic acid (DTPA) images in a patient with hypertension receiving captopril therapy. A repeat DTPA renogram was performed after stopping captopril therapy, which revealed normal bilateral DTPA uptake.44 Several theories have been proposed for explaining this mechanism. Normally, a balance maintains glomerular filtration based on using vascular tone between the preglomerular and postglomerular arterioles. In the presence of significant renal artery stenosis, this balance is disturbed, because pressure in the preglomerular arteriole is decreased and the filtration pressure can be maintained only by the postglomerular arteriolar vasoconstriction by the renin angiotensin system. The administration of ACE inhibitor, such as captopril, prevents the conversion of angiotensin I to the active vasoconstrictor angiotensin II and angiotensin III. By inhibiting the compensatory increase in vascular tone at the postglomerular arteriole, ACE inhibitors decrease the glomerular filtration in the presence of renal artery stenosis. The administration of ACE inhibitors along with radionuclide renography provide a noninvasive method for the detection of functionally significant renal artery stenosis.45,46 Various criteria have been put forth for interpreting the results depending on the type of tracer used. The basis of all methods of renal scintigraphy for the detection of renal artery stenosis is to demonstrate delayed and decreased total activity over the affected kidney. False-positive results may be seen in diseases that cause unilateral reduction in blood flow, including chronic pyelonephritis, urinary obstruction, renal vein thrombosis, renal hilar compression, perirenal abscess, or hematoma. False-negative results can be seen after the long-term administration of captopril, over hydration, and in bilateral renal artery stenosis. The study is nondiagnostic in patients with poor renal function. Overall, the usefulness of ACE scintigraphy as a screening test for hemodynamically significant renal artery stenosis is questionable, although a positive result is a strong predictor of those patients who may respond to intervention.47

Catheter Angiography Conventional angiography is considered the reference standard for the detection of renal artery stenosis. Intra-arterial

279 Table 3 Etiologies of Renal Artery Dissection Atherosclerosis Fibromuscular dysplasia Extension of aortic dissection Trauma (deceleration) Marfan syndrome Ehlers-Danlos syndrome Iatrogenic Idiopathic

angiography is an invasive procedure most commonly performed through femoral artery puncture under local anesthesia. Transradial, transbrachial, and transaxillary approaches may be used if femoral approach is unsuccessful. Flush abdominal angiogram is obtained with a 5-French pigtail catheter with the tip of catheter above the level of renal arteries. Commonly, selective renal angiograms are obtained. The images are obtained at appropriate obliquities to demonstrate the optimal visualization of the vessel origins. Approximately 50-120 mL of nonionic iodinated contrast media is generally used. Angiography provides good anatomic details and delineates vessel variants. Both the angiographic and the nephrographic phases can be evaluated; the latter may help demonstrate any ischemic changes. Unlike the other techniques, a concurrent therapeutic procedure can be performed at the same sitting. However, there are possible disadvantages associated with this technique, such as puncture-related hematomas, dissection, emboli, contrast-related reactions, its invasive nature, and use of ionizing radiation. Other important aspects are failure to give information on the state of the vessel wall and lack of functional assessment through the stenotic segment.

Renal Artery Dissection and Renal Vascular Pedicle Injury Renal artery dissection occurs when layers of the arterial wall become separated. Renal artery dissections are stenotic or occlusive lesions most often observed in hypertensive patients with underlying atherosclerosis or fibromuscular disease. They are usually seen in the third to sixth decade and are 4 times more common in men. Bilateral renal artery dissection has been seen in 12% of these patients.48 Small renal artery dissections are usually clinically silent, but larger dissections may present as flank pain, hematuria, renal infarction, and hypertension. Renal artery involvement by aortic dissection may compromise the flow to the kidney, resulting in the same clinical manifestations as other causes of renal artery stenosis. Renal artery dissection may be due to a variety of causes (Table 3). The typical imaging finding, regardless of modality, is the appearance of 2 separate lumens within the artery, although 1 lumen may occlude. Doppler ultrasound is often the firstline evaluation of renovascular hypertension and may demonstrate narrowed lumen of renal artery and signs of global ischemia. CTA is a valuable tool to show asymmetry of renal

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Figure 11 Aortic dissection with renal infarction. (A) Axial contrast-enhanced CT image in a trauma patient demonstrates intimal flap (arrow) within the proximal abdominal aorta. (B) Image at the level of the right renal artery shows global ischemia of the right kidney. The proximal right renal artery shows contrast opacification (arrow) beyond which it is not well demonstrated (arrowheads).

enhancement (Fig. 11) and can display the entire extent of the dissection and the re-entry site. Its superior resolution allows it to characterize intrarenal dissection better than MR methods. While CT cannot quantify the renal function as MR does, substantial information can be obtained from the pattern of parenchymal enhancement. 3D gadolinium-enhanced MRA is a useful technique for evaluating dissection in stable patients and for follow-up studies. MR flow measurements are a good approach to differentiate between a thrombosed lumen and slow flow, as thrombi may show various signal intensities depending on their age. While even slow flow shows some phase shift in MR flow measurements, thrombus does not. However, motion along with the small lumen of distal renal vessels makes accurate measurements in these vessels quite challenging. Another approach is the use of time-resolved multiphase MRA, which shows the arrival of contrast agent in the different lumens and thus allows assessing the origin of the renal blood supply. With the aid of multiplanar reformations and subvolume MIP images, it is possible to diagnose the type of aortic dissection, differentiate slow flow from thrombus, recognize entry and reentry tears, and identify visceral and renal artery involvement.49 Renal pedicle injury is usually associated with decelerationrelated blunt injury. This can result in dissection of the main renal artery or vein. Occasionally, penetrating injuries can lacerate or transect the renal vessels. The usual clinical presentation is hypotension with massive hemorrhage; these patients are hemodynamically unstable. If the diagnosis is made within 3-6 hours of the injury, surgical revascularization of the affected kidney may be attempted. Often, the kidney is irreparably injured, and revascularization is not possible. Nephrectomy is commonly the required treatment. CT is the standard imaging modality as a part of trauma scanning. The common imaging findings of arterial injury

include extensive perirenal hemorrhage, delayed and diminished nephrogram, rim nephrogram, and diminished opacification of the lateral segment of main renal artery. Persistent nephrogram is seen in renal vein thrombosis. Power Doppler may show asymmetric absence of flow in the parenchyma of the affected kidney. Flow in a patent accessory artery may hinder the sonographic diagnosis. However, the sensitivity of ultrasound for genitourinary trauma is low compared to CT.50

Renal Infarct Renal infarction is defined as a localized or global area of ischemic necrosis of kidney, resulting most often from sudden occlusion of its arterial supply. The most common cause is thromboembolism, usually of cardiac origin, but various other causes are possible (Table 4). Renal infarction can occur at any age with no sex predilection. The classical clinical presentation is sudden onset of flank pain or back pain. Hematuria, proteinuria, fever, and leukocytosis may also be associated features. Hypertension can be seen in chronic infarction. Imaging appearances vary depending on the age at onset, anatomy, and vascular distribution. They can be classified as focal (segmental or subsegmental), and global. Ultrasound examination may be nonspecific. Color Doppler may show focal or global absence of blood flow in the involved kidney. Chronically, there may be scarring with retraction of the cortical margin. On CT, focal acute infarcts appear as wedge-shaped nonenhancing areas within an otherwise normal-appearing kidney (Fig. 12). “Cortical rim sign” due to enhancement of the renal margin by capsular arteries is a reliable indicator of subacute infarction but may not be visible in the first 8 hours after infarction occurs.51 In cases of global infarction, kidney

Renovascular imaging Table 4 Causes of Renal Infarction Embolism: Cardiac (most common), rheumatic, arrhythmia, myocardial infarction, prosthetic valve, subacute bacterial endocarditis Thrombosis: Atherosclerosis Sickle cell disease Polyarteritis nodosa Drug-induced vasculitis Thrombocytopenic purpura Thromboangitis obliterans Aneurysm or dissection of renal artery or extension from aorta Trauma: Blunt or penetrating Surgery or interventional procedures Paraneoplastic syndrome Hypercoagulable states Acute venous occlusion

is initially enlarged due to edema and has preserved reniform configuration. The affected kidney shows lack of enhancement and no excretion of contrast. Medullary striations can be seen in the form of “spoke-wheel” pattern of enhancement due to collateral circulation. As the infarct becomes chronic, atrophy begins to start with irregular renal contour secondary to scar tissue. Perinephric manifestations are uncommon with infarcts. On MRI, infarcts usually demonstrate low signal intensity on both T1- and T2-weighted images. No enhancement is seen on post contrast images. The mimics of infarcts include acute pyelonephritis, vasculitis, and trauma. The presence of perinephric findings or pelvicalyceal abnormalities favors pyelonephritis. Clinical history is important to differentiate infarcts from vasculitis.

281 Table 5 Underlying Etiologies Associated with Renal Artery Aneurysm Atherosclerotic disease (the most common cause) Fibromuscular dysplasia Wegener’s granulomatosis Neurofibromatosis Pregnancy Mycotic aneurysms Iatrogenic and traumatic injury

Renal Artery Aneurysm/Pseudoaneurysm The prevalence of renal artery aneurysms is 1%. Most renal artery aneurysms are seen in the fourth and fifth decades of life with a female predilection.52 Although there are many possible causes (Table 5), most aneurysms are seen in the main renal artery or at the bifurcation of renal artery where congenital anomalies are most common and flow disturbances due to plaques may also be present. Extraparenchymal aneurysms, such as those at the bifurcation, comprise approximately 85% of all renal artery aneurysms; the rest are intraparenchymal. Most renal artery aneurysms are saccular (80%) and noncalcified (82%).52 Multiple small intrarenal aneurysms are usually associated with polyarteritis nodosa or fungal infections, such as mycotic aneurysms in intravenous drug abusers. Renal pseudoaneurysms, or contained ruptures of the arterial wall, are usually secondary to inflammation and trauma. Most renal artery aneurysms are asymptomatic and are usually detected incidentally on radiologic imaging with a small risk of rupture. The decision to treat a renal artery aneurysm is based on size and risk of rupture. For aneurysms less than 2 cm, follow-up imaging with CT or MR imaging is

Figure 12 Renal infarct. (A) Axial contrast-enhanced CT image in hypertensive patient with pain shows incomplete opacification of mid left renal artery (arrow). (B) At an adjacent level, there is focal geographic nonenhancing parenchyma (arrowheads) and reactive mild perinephric stranding.

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Figure 13 Renal artery pseudoaneurysm. (A) Grayscale ultrasound of a renal transplant allograft shows round anechoic lesion (calipers), possibly cyst. (B) Longitudinal color Doppler of the renal artery shows typical “yin-yang” appearance of circular blood flow, classic for pseudoaneurysm. (Color version of figure is available online.)

appropriate. However, in a pregnant patient with spontaneous retroperitoneal hematoma, the increased possibility of rupture should be considered.53 Pseudoaneurysms require more acute therapy due to their increased risk of hemorrhage. Radiologic imaging is essential for pre-interventional planning or follow-up care. Ultrasound is least invasive and easily available and may serve as initial imaging investigation. The aneurysm appears as a hypo- to anechoic structure with or without calcification. For pseudoaneurysms, calcifications would not be expected due to the short time course. Color Doppler exhibits classic circular color flow known as “yinyang” sign (Fig. 13). Mural thrombus is seen as hypoechoic without color filling on Doppler. On spectral Doppler, the classic to-and-fro flow is difficult to demonstrate because the abnormality is much deeper in comparison to the groin. The waveforms from the aneurysm lumen usually demonstrate low-velocity signals that are pulsatile but do not appear classically arterial in nature unless the spectrum is obtained close to the entering jet. CT scan is a reproducible modality for diagnosis and follow-up. CTA with the additional imaging planes is particularly useful in detecting intrapelvic and intraparenchymal aneurysms involving the main or hilar arteries. CTA with volume-rendering techniques can demonstrate the origin and extent of the aneurysm and its relationship to the other vessels. Presence of mural thrombus predisposes the kidney to infarcts. Axial, MIP, and volume rendering images can give detailed information about location, type, calcification, and thrombosis of renal arterial aneurysms (Fig. 14). The risk of rupture is small, particularly when rim-like calcification is present in the wall of aneurysm.54 It is difficult to predict at what size a renal artery aneurysm is prone to rupture and should be repaired. Many surgeons use 1.5-2.0 cm as a criteria for operative intervention; others use 3.0-4.0 cm.55,56 It has been suggested that calcifications within the wall reduce the risk factors for rupture.57 Thus, demonstration of size and

calcifications in renal artery aneurysms is important. CTA is probably associated with a diagnostic accuracy similar to that of conventional angiography, with the added benefits of being a quicker, more cost-effective, and noninvasive method for the evaluation of the renal vasculature.58 Contrast-enhanced MRA can reliably identify renal artery aneurysms; however, MRA cannot give as detailed information about the aneurysmal wall or calcifications. Large aneurysms and those affecting the main renal arteries or large segmental branches can be well seen on 3D gadolinium MRA images. Because of its limited spatial resolution, however, the depiction of small intrarenal aneurysms of polyarteritis nodosa may be less reliable.

Renal Arteriovenous Communications Arteriovenous (AV) communications are direct communications from an artery to a vein without an intervening capillary bed. They are of 2 types: (1) congenital and (2) acquired. Approximately 75% of AV communications are acquired; the rest are congenital.59 Types include AV fistula and AV malformation. AV fistulas are acquired lesions with a single communication between an artery and a vein, whereas AV malformations are congenital lesions with multiple, large arterial feeding vessels and numerous arteriovenous communications. Arteriovenous fistulas comprise 70%-80% of communications in the kidney.60 AV fistulas can result from trauma, surgery, tumors, inflammation, or erosion of an aneurysm directly into the vein. AV fistulas have a male preponderance. Small AV fistulas are asymptomatic, but the larger ones may present with abnormal bruit, and hematuria. Ischemia in the renal parenchyma distal to the arteriovenous fistula may induce renin-mediated hypertension and impaired renal function.61 Postbiopsy fistulas can be seen in up to 16% of trans-

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283 of lighter colors (Fig. 15). Spectral Doppler shows large peak systolic and end-diastolic frequency shifts with a lower resistive index than those of a normal intrarenal artery. Renal AVMs can be intraparenchymal or within the renal sinus. On contrast-enhanced CT, it may rarely be difficult to differentiate AVM from renal cell carcinoma since both show enhancement. Doppler ultrasound can confirm the mass to be AVM when the typical flow pattern is seen within the mass. The CT appearances depend on the timing of image acquisition relative to contrast material administration, amount of contrast material, and injection rate. Contrasted CT performed in the vascular and early corticomedullary phases is important in the detection of intrarenal vascular mass with feeding arteries and veins (Fig. 15). AVMs may bleed causing parenchymal, subcapsular, or perinephric hematoma. MR can be performed in cases of poor renal function. Unenhanced MRI can demonstrate AVM as flow voids on conventional images. Heavy T2-weighted sequences have been reported to have high accuracy in defining the extent of vascular malformation. MR is helpful in differentiating the AVM from the mass lesion by showing flow voids in the lesion. Angiography is the reference standard for establishing the diagnosis of AVM. It demonstrates the detailed anatomy of feeding arteries and veins, which facilitates accurate planning before therapeutic intervention.

Renal Vein Thrombosis

Figure 14 Renal artery aneurysm. (A) Contrast-enhanced coronal maximum intensity projection image shows an extraparenchymal round vascular lesion near the renal artery bifurcation (arrow). (B) Volume-rendered CT image demonstrates the anatomical details of the aneurysm (asterisk) and the right renal artery origin from the aorta (arrow). RA, renal artery. (Color version of figure is available online.)

plant kidneys. Most of them resolve spontaneously, and few need intervention.62 On grayscale ultrasound, arteriovenous malformations (AVMs) simulate hydronephrosis and cysts. On color Doppler, AVMs show coarse, mosaic vibrational artifacts or modulation of the Doppler signal from the artery and vein.63 They may also be seen as focal areas of flow, portrayed as a mixing

Renal vein thrombosis usually results secondary to underlying renal abnormality of the kidney, hydration, or coagulation status (Table 6). The left renal vein is more commonly involved, probably because of its longer length. Classical acute presentation is flank pain and hematuria. With more chronic onset, symptoms are nonspecific. Sonography is the most commonly used initial modality for diagnosis of renal vein thrombosis. In cases of acute renal vein thrombosis, kidneys may be enlarged and hypoechoic, with loss of corticomedullary differentiation. Acutely, it may be anechoic or hypoechoic (Fig. 16). Chronic thrombus may be echogenic or calcified. Doppler should show decreased or absent venous flow. Absent or reversed end-diastolic flow in intraparenchymal native renal arteries may represent indirect evidence of acute renal vein thrombosis. However, negative arterial Doppler in a clinical setting of renal vein thrombosis warrants further imaging due to low sensitivity of 40%.64 Contrast-enhanced CT shows acute thrombus as a filling defect in thick-walled dilated renal vein. In addition, the kidney may be enlarged, with edema in the renal sinus and perinephric space. The nephrogram shows coarse striations with delayed onset of nephrographic phase (Fig. 17). In chronic renal vein thrombosis, the affected renal vein has smaller caliber due to retraction of the clot. Extensive collaterals develop in perirenal region and also along the proximal to middle ureter.65 Thrombus associated with malignancy usually shows inhomogeneous enhancement. In cases of tumor thrombus, it is important to identify any superior extension into IVC. The portion of IVC just above the renal veins

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Figure 15 Renal AVM. (A) Contrast-enhanced axial CT image shows enhancing tubular opacities in left parahilar region (arrowheads). (B) On adjacent image, the tubular opacities extend into a dilated left renal vein (arrow). (C) Transverse color Doppler sonography of the kidney shows turbulent flow within this lesion (large arrow) surrounded by a hypoechoic avascular region (smaller arrows), suggesting AVM with mural thrombosis. (Color version of figure is available online.)

frequently appears inhomogeneous on early phase contrastenhanced scans due to mixing artifacts. Therefore, multiplanar reconstruction images on CT or MRI help to demonstrate the extension of thrombus into IVC (Fig. 18). Delayed scans may also be helpful to improve the visualization of IVC. MRI serves as a problem-solving tool especially in cases where superior extension of the thrombus is difficult to assess on CT images (Fig. 18). MRI produces high-contrast images between flowing blood, vascular walls, and surrounding tissue. The major benefit is the avoidance of radiation and intravenous contrast material. MR reveals low signal intensity of the renal parenchyma on both T1 and T2 sequences and also compression of collection system. In acute renal vein thrombosis, a low signal intensity band can be seen at the outer part of medulla due to hemorrhage caused by impaired blood drainage. In chronic renal vein thrombosis, extensive collaterals arise from the renal hilum around the proximal ureter and capsular vessels. The left gonadal vein may also be dilated.

Vasculitis A diverse group of diseases categorized as vasculitis typically affects small and medium-sized vessels. They are primarily of autoimmune origin, affecting various organs. The kidney is the most frequently affected organ. The most common entity is polyarteritis nodosa, followed by systemic lupus erythematosus, rheumatoid arthritis, Wegener’s granulomatosis, and drug-induced vasculitis. It is difficult to distinguish between various diseases with radiologic investigations.

Polyarteritis Nodosa Polyarteritis nodosa is a vasculitis that usually involves medium-sized vessels. Renal involvement is seen in 90% of patients.66 Clinical presentation includes fever, abdominal pain, hematuria, and hypertension. Pathologically, the vascular wall may rupture, thereby resulting in small foci of hemorrhage. Subsequent inflammation and scarring can result in vascular irregularity, truncation, microaneurysms,

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and infarction. The arteriographic findings correlate well with pathologic findings. The presence of small aneurysms at the bifurcation of the interlobar or arcuate arteries is a characteristic finding. Occasionally, these microaneurysms may be seen on imaging. Contrast-enhanced CT usually shows areas of infarction of different ages. The contour of kidneys may appear scarred. Multiple linear bands of decreased attenuation may be seen because of occlusion of small intrarenal arteries.67 Occasionally, small aneurysms may rupture and produce intrarenal, subcapsular, or perinephric hematoma.61

Systemic Lupus Erythematosus Renal disease occurs in 30%-50% of patients with systemic lupus erythematosus.65 It can involve glomerular, tubular, or vascular components, and the incidence of renal vein thrombosis is markedly increased. Angiographic and CT findings are similar to that of polyarteritis nodosa. Renal size varies depending on the stage of lupus nephritis. Doppler ultrasound demonstrates nonfilling or incomplete filling of the renal vein. Renal vein thrombosis is seen as a filling defect on contrast-enhanced CT and may also show extension into IVC. In longstanding thrombosis, collateral vessels may be seen in hilar region and also along the proximal part of ureter. These may be a source of false-negative Doppler results.

Table 6 Etiologies Associated with Renal Vein Thrombosis Inherited hypercoagulable states Deficiency of antithrombin III, protein S, protein C Other hypercoagulable states Pregnancy Disseminated malignancy Nephrotic syndrome Systemic disease Systemic lupus erythematosus Sickle cell anemia Diabetes mellitus Polyarteritis nodosa Dehydration Tumor extension Renal cell carcinoma Wilms’ tumor Transitional cell carcinoma Adrenal tumor Renal angiomyolipoma Iatrogenic Drugs (oral contraceptive pills, estrogen) Renal transplant rejection Thrombus extension Ovarian vein thrombosis Deep vein thrombosis Mechanical compression Retroperitoneal fibrosis Tumor Hematoma Aberrant vessels

Figure 16 Renal vein thrombosis. Grayscale ultrasound image in patient with pain and hematuria shows dilated right renal vein filled with predominantly hypoechoic material (small arrows) extending into the inferior vena cava, suggesting acute thrombus. Hyperechoic material is also attached along the anterior wall indicating of chronic nature of part of thrombus (asterisk). Note is also made of enlarged, echogenic kidney (large arrow), which can be occasionally seen in renal vein thrombosis.

Drug-induced Vasculitis Vasculitis associated with multiple drug abuse may morphologically and angiographically resemble polyarteritis nodosa. Methamphetamine is one of the commonest offending drugs, but most patients are also exposed to other drugs, such as cocaine. Certain chemotherapeutic agents as vinblastine, cisplatin, and bleomycin have been associated with vasculitis.68 CT may demonstrate renal infarcts of various size, number, and age. Occasionally, a mycotic aneurysm may also be seen.

Figure 17 Renal vein thrombosis. Contrast-enhanced axial CT demonstrates enlarged, heterogeneous right kidney with striated nephrogram (arrows) caused by thrombus seen as a filling defect in the right renal vein (arrowheads).

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Figure 18 Extension of renal vein thrombus into inferior vena cava (IVC). (A, B) Contrast-enhanced axial CT images show a dilated thrombosed left renal vein (arrowheads) extending into the IVC, which is also dilated with thrombus (arrow). (C) Image at a more cranial level suggests extension of thrombus into the right atrium (arrow). (D) Coronal contrast-enhanced T1-weighted MR image confirms IVC thrombus extending into right atrium (arrows). Also seen is a large right renal mass (M) and hepatic metastasis (asterisk).

Summary As more options arise for the noninvasive diagnosis of genitourinary disease, selection of the proper imaging modality becomes all the more important. For vascular diagnosis, the judicial use of ultrasound, CT, and MRI can usually lead to the correct diagnosis and guide clinical management. However, success relies on the application of reasonable threshold values and an understanding of the limitations and uncertainty that each imaging technique occasionally encounters.

Acknowledgment Special thanks to Toni Braddy for assistance in manuscript preparation.

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